Control Of Redox State Research Articles

Control of the Hydroquinone/Benzoquinone Redox State in High-Mobility Semiconducting Conjugated Coordination Polymers.

Conjugated coordination polymers (c-CPs) are unique organic-inorganic hybrid semiconductors with intrinsically high electrical conductivity and excellent charge carrier mobility. However, it remains a challenge in tailoring electronic structures, due to the lack of clear guidelines. Here, we develop a strategy wherein controlling the redox state of hydroquinone/benzoquinone (HQ/BQ) ligands allows for the modulation of the electronic structure of c-CPs while maintaining the structural topology. The redox-state control is achieved by reacting the ligand TTHQ (TTHQ=1,2,4,5-tetrathiolhydroquinone) with silver acetate and silver nitrate, yielding Ag4TTHQ and Ag4TTBQ (TTBQ=1,2,4,5-tetrathiolbenzoquinone), respectively. In spite of sharing the same topology consisting of a two-dimensional Ag-S network and HQ/BQ layer, they exhibit different band gaps (1.5 eV for Ag4TTHQ and 0.5 eV for Ag4TTBQ) and conductivities (0.4 S/cm for Ag4TTHQ and 10 S/cm for Ag4TTBQ). DFT calculations reveal that these differences arise from the ligand oxidation state inhibiting energy band formation near the Fermi level in Ag4TTHQ. Consequently, Ag4TTHQ displays a high Seebeck coefficient of 330 μV/K and a power factor of 10 μW/m ⋅ K2, surpassing Ag4TTBQ and the other reported silver-based c-CPs. Furthermore, terahertz spectroscopy demonstrates high charge mobilities exceeding 130 cm2/V ⋅ s in both Ag4TTHQ and Ag4TTBQ.

Cross-Talk Between Selenium Nanoparticles and Cancer Treatment Through Autophagy.

Autophagy is commonly referred as self-eating and a complex cellular process that is involved in the digestion of protein and damaged organelles through a lysosome-dependent mechanism, and this mechanism is essential for maintaining proper cellular homeostasis. Selenium is a vital trace element that plays essential functions in antioxidant defense, redox state control, and range of particular metabolic processes. Selenium nanoparticles have become known as a promising agent for biomedical use, because of their high bioavailability, low toxicity, and degradability. However, and in recent years, they have attracted the interest of researchers in developing anticancer nano-drugs. Selenium nanoparticles can be used as a potential therapeutic agent or in combination with other agents to act as carriers for the development of new treatments. More intriguingly, selenium nanoparticles have been extensively shown to impact autophagy signaling, allowing selenium nanoparticles to be used as possible cancer treatment agents. This review explored the connections between selenium and autophagy, followed by developments and current advances of selenium nanoparticles for autophagy control in various clinical circumstances. Furthermore, this study examined the functions and possible processes of selenium nanoparticles in autophagy regulation, which may help us understand how selenium nanoparticles regulate autophagy for the potential cancer treatment.

PGR5-LIKE PHOTOSYNTHETIC PHENOTYPE1A redox states alleviate photoinhibition during changes in light intensity.

Plants have evolved photosynthetic regulatory mechanisms to maintain homeostasis in response to light changes during diurnal transitions and those caused by passing clouds or by wind. One such adaptation directs photosynthetic electron flow to a cyclic pathway to alleviate excess energy surges. Here, we assign a function to regulatory cysteines of PGR5-like protein 1A (PGRL1A), a constituent of the PROTON GRADIENT REGULATION5 (PGR5)-dependent cyclic electron flow (CEF) pathway. During step increases from darkness to low light intensity in Arabidopsis (Arabidopsis thaliana), the intermolecular disulfide of the PGRL1A 59-kDa complex was reduced transiently within seconds to the 28-kDa form. In contrast, step increases from darkness to high light stimulated a stable, partially reduced redox state in PGRL1A. Mutations of 2 cysteines in PGRL1A, Cys82 and Cys183, resulted in a constitutively pseudo-reduced state. The mutant displayed higher proton motive force (PMF) and nonphotochemical quenching (NPQ) than the wild type (WT) and showed altered donor and acceptor dynamic flow around PSI. These changes were found to correspond with the redox state of PGRL1A. Continuous light regimes did not affect mutant growth compared to the WT. However, under fluctuating regimes of high light, the mutant showed better growth than the WT. In contrast, in fluctuating regimes of low light, the mutant displayed a growth penalty that can be attributed to constant stimulation of CEF under low light. Treatment with photosynthetic inhibitors indicated that PGRL1A redox state control depends on the penultimate Fd redox state. Our results showed that redox state changes in PGRL1A are crucial to optimize photosynthesis.

Selenium influences thyroid hormones, myricetin has anti-cancer effects on human papillary thyroid cancer cells, and thyroid hormones have been associated with psychological disorders: Thyroid evaluation and therapy during pregnancy

Introduction: A micronutrient called selenium; a non-metallic element is necessary to manufacture selenoproteins, including selenocysteine. The thyroid has the highest concentration of selenium per gram of tissue in people. The majority of known selenoproteins, including glutathione peroxidase, are expressed in the thyroid and are crucial for the metabolism of thyroid hormones, control of redox states, and preservation of cellular homeostasis. It has been demonstrated that selenium therapy for Graves orbitopathy patients can slow the disease's course and enhance the quality of life. Different selenium supplements have demonstrated varying anticancer efficacy in thyroid cancer. It also looked at how different treatment plans affected patients' thyroid function, mood, and inflammatory markers. TSH (thyroid-stimulating hormone) is slightly elevated in subclinical hypothyroidism, while T4 or T3 levels are normal. Objective: The purpose of this study was to evaluate the therapeutic effects of levothyroxine sodium given alone or in combination with selenium on patients with chronic lymphocytic thyroiditis and hypothyroidism to serve as a guide for clinical treatment. The purpose of the current study is to ascertain the impact of selenium supplementation on thyroid hormone and anti-thyroid peroxidase antibody (anti-TPO AB) levels. The pathophysiology of this illness may be affected by the imbalance in the activity of T cells such as Th1, Th2, Th17, and Treg. This study was to evaluate any changes in the release of cytokines by these cells after selenium administration in patients with HT. The diagnosis and management of thyroid problems during pregnancy are covered in detail in this article. It also includes a summary of the main recommendations made by several medical associations for the diagnosis, treatment, and interpretation of thyroid function during pregnancy. Results: The combined group's overall effective rate was much greater than the control group's. After therapy, both groups' TT3, TT4, TSH, TgAb, and TPOAb levels, SAS and SDS scores, and levels of inflammatory mediators such as IL-2, IL-10, and TNF- all showed a significant improvement. In the combination group, IL-10 levels increased more, and TGAb, TPOAb, IL-2, TNF-, SAS, and SDS scores reduced more when compared to the control group, whereas the differences in the other indices were not statistically significant. According to research, LT4 has some efficacy in treating CLT with hypothyroidism, and selenium therapy in combination with LT4 can increase its therapeutic effect and help patients' immunological and inflammatory responses as well as their mood. Conclusions: Myo-inositol, vitamin D, and selenium supplementation together had an impact on the decline in cytokine markers, Ab-TPO, and Ab-TG levels, which helped to compensate for the underlying condition. Since myricetin is a strong inducer of HATC cell death, it may be helpful in the creation of HATC therapeutic medicines. Myricetin significantly reduced the growth of HATC cells, by almost 70%. A significant number of dead cells showed sub-G1 phase arrest. In SNU-80 HATC cells, myricetin similarly displayed cytotoxicity and caused DNA condensation in a dose-dependent manner. Additionally, myricetin induced the mitochondria to release apoptosis-inducing factor (AIF) into the cytoplasm and changed the potential of the mitochondrial membrane.

Electrochemical atomic force microscopy of two-dimensional trinuclear ruthenium clusters molecular assembly and dynamics under redox state control.

Mixed-valence ruthenium trinuclear clusters containing dichloroacetates were synthesized, and the self-assembly of a single molecular adlayer composed of these clusters on a graphite surface was investigated by atomic force microscopy (AFM). AFM clearly revealed the dynamics of two-dimensional (2D) structure formation as well as the molecular characteristics of the adlayers at different electrochemical interfaces. The results verified that the design of metal complexes is important not only for redox chemistry but also for molecular assembly and nanoarchitecture construction.

Homeostatic control of redox status and health.

Research on oxidants and electrophiles has shifted from focusing on damage to biomolecules to the more fine-grained physiological arena. Redox transitions as excursions from a steady-state redox set point are continually ongoing in maintenance of redox balance. Current excitement on these topics results from the fact that recent research provided mechanistic insight, which gives rise to more concrete and differentiated questions. This Commentary focuses on redox eustress and the feedback restoration of steady state as concepts in active maintenance of physiological health, with brief discussion of redox stress response to viral infection, exemplified by COVID-19.

Control of Oxidative Stress in Cancer Chemoresistance: Spotlight on Nrf2 Role.

Chemoresistance represents the main obstacle to cancer treatment with both conventional and targeted therapy. Beyond specific molecular alterations, which can lead to targeted therapy, metabolic remodeling, including the control of redox status, plays an important role in cancer cell survival following therapy. Although cancer cells generally have a high basal reactive oxygen species (ROS) level, which makes them more susceptible than normal cells to a further increase of ROS, chemoresistant cancer cells become highly adapted to intrinsic or drug-induced oxidative stress by upregulating their antioxidant systems. The antioxidant response is principally mediated by the transcription factor Nrf2, which has been considered the master regulator of antioxidant and cytoprotective genes. Nrf2 expression is often increased in several types of chemoresistant cancer cells, and its expression is mediated by diverse mechanisms. In addition to Nrf2, other transcription factors and transcriptional coactivators can participate to maintain the high antioxidant levels in chemo and radio-resistant cancer cells. The control of expression and function of these molecules has been recently deepened to identify which of these could be used as a new therapeutic target in the treatment of tumors resistant to conventional therapy. In this review, we report the more recent advances in the study of Nrf2 regulation in chemoresistant cancers and the role played by other transcription factors and transcriptional coactivators in the control of antioxidant responses in chemoresistant cancer cells.

Redox State Control of Human Cytoglobin by Direct Electrochemical Method to Investigate Its Function in Molecular Basis

The direct electron transfer between human cytoglobin (Cygb) and the electrode surface, which would allow manipulating the oxidation states of the heme iron in Cygb, was first observed by immobilizing Cygb on a nanoporous gold (NPG) electrode via a carboxy-terminated alkanethiol. The voltammetric performances of the wild type and mutated Cygb-immobilized NPG electrodes were evaluated in the absence or presence of potential substrates. The obtained results demonstrated that the usefulness of the proposed method in understanding the function of Cygb in molecular basis.

Redox Control of Charge Transport in Vertical Ferrocene Molecular Tunnel Junctions

Summary Controlling charge transport through molecular tunnel junctions is of crucial importance for exploring basic physical and chemical mechanisms at the molecular level and realizing the applications of molecular devices. Here, through a combined experimental and theoretical investigation, we demonstrate redox control of cross-plane charge transport in a vertical gold/self-assembled monolayer (SAM)/graphene tunnel junction composed of a ferrocene-based SAM. When an oxidant/reductant or electrochemical control is applied to the outside surface of the neutral single-layer graphene top electrode, reversible redox reactions of ferrocene groups take place with charges crossing the graphene layer. This leads to counter anions on the outer surface of graphene, which balance the charges of ferrocene cations in the oxidized state. Correspondingly, the junctions switch between a high-conductance, neutral state with asymmetrical characteristics and a low-conductance, oxidized state with symmetrical characteristics, yielding a large on/off ratio (>100).

A key metabolic integrator, coenzyme A, modulates the activity of peroxiredoxin 5 via covalent modification

Peroxiredoxins (Prdxs) are antioxidant enzymes that catalyse the breakdown of peroxides and regulate redox activity in the cell. Peroxiredoxin 5 (Prdx5) is a unique member of Prdxs, which displays a wider subcellular distribution and substrate specificity and exhibits a different catalytic mechanism when compared to other members of the family. Here, the role of a key metabolic integrator coenzyme A (CoA) in modulating the activity of Prdx5 was investigated. We report for the first time a novel mode of Prdx5 regulation mediated via covalent and reversible attachment of CoA (CoAlation) in cellular response to oxidative and metabolic stress. The site of CoAlation in endogenous Prdx5 was mapped by mass spectrometry to peroxidatic cysteine 48. By employing an in vitro CoAlation assay, we showed that Prdx5 peroxidase activity is inhibited by covalent interaction with CoA in a dithiothreitol-sensitive manner. Collectively, these results reveal that human Prdx5 is a substrate for CoAlation in vitro and in vivo, and provide new insight into metabolic control of redox status in mammalian cells.

Single-molecule study of redox control involved in establishing the spinach plastocyanin-cytochrome b6f electron transfer complex

Small diffusible redox proteins play a ubiquitous role in bioenergetic systems, facilitating electron transfer (ET) between membrane bound complexes. Sustaining high ET turnover rates requires that the association between extrinsic and membrane-bound partners is highly specific, yet also sufficiently weak to promote rapid post-ET separation. In oxygenic photosynthesis the small soluble electron carrier protein plastocyanin (Pc) shuttles electrons between the membrane integral cytochrome b6f (cytb6f) and photosystem I (PSI) complexes. Here we use peak-force quantitative nanomechanical mapping (PF-QNM) atomic force microscopy (AFM) to quantify the dynamic forces involved in transient interactions between cognate ET partners. An AFM probe functionalised with Pc molecules is brought into contact with cytb6f complexes, immobilised on a planar silicon surface. PF-QNM interrogates the unbinding force of the cytb6f-Pc interactions at the single molecule level with picoNewton force resolution and on a time scale comparable to the ET time in vivo (ca. 120 μs). Using this approach, we show that although the unbinding force remains unchanged the interaction frequency increases over five-fold when Pc and cytb6f are in opposite redox states, so complementary charges on the cytb6f and Pc cofactors likely contribute to the electrostatic forces that initiate formation of the ET complex. These results suggest that formation of the docking interface is under redox state control, which lowers the probability of unproductive encounters between Pc and cytb6f molecules in the same redox state, ensuring the efficiency and directionality of this central reaction in the ‘Z-scheme’ of photosynthetic ET.

36-OR: Energy Stress Restores Muscle Insulin Action in High-Fat (HF)-Fed SIRT3 KO Mice

SIRT3 is a mitochondrial deacetylase that is necessary for insulin-stimulated muscle glucose uptake (MGU) in the setting of overnutrition, and its action is redox state-dependent (NAD/NADH). Energy stress induced by AICAR administration increases muscle insulin action and glucose uptake while enhancing the control of redox state. We hypothesized that acute energy stress would exacerbate the impairment in insulin-stimulated MGU in high fat-fed (HF) SIRT3 KO mice. To test this hypothesis, HF SIRT3 KO and WT littermates underwent 4h of either AICAR (1mg/kg/min) to induce an energetic stress or saline infusion followed by hyperinsulinemic (4mU/kg/min) euglycemic clamps. Experiments were conducted one week post jugular vein and carotid artery catheterization. Insulin clamps were combined with [3-3H] glucose to measure glucose fluxes and 2[14C]deoxyglucose to assess an index of MGU. AICAR significantly improved insulin sensitivity of liver, but not muscle of HF WT mice. Saline-SIRT3 KO mice were more insulin resistant than saline-WT mice, as glucose infusion rate (GIR) and MGU were reduced by ~50%. AICAR completely abolished the added insulin resistance in SIRT3 KO mice as GIR was similar to AICAR-WT. Consistent with this, AICAR increased muscle insulin-stimulated MGU in the SIRT3 KO mice to levels observed in WT mice. Results show that energy stress induced by AICAR infusion was sufficient to circumvent the defect in insulin-stimulated glucose uptake induced by SIRT3 KO, possibly by rescuing redox handling in skeletal muscle. Disclosure L. Lantier: None. C.C. Hughey: None. D. Wasserman: None. Funding National Institutes of Health (DK54902)

Redox control and autoxidation of class 1, 2 and 3 phytoglobins from Arabidopsis thaliana

Despite a recent increase in interest towards phytoglobins and their importance in plants, much is still unknown regarding their biochemical/biophysical properties and physiological roles. The present study presents data on three recombinant Arabidopsis phytoglobins in terms of their UV-vis and Raman spectroscopic characteristics, redox state control, redox potentials and autoxidation rates. The latter are strongly influenced by pH for all three hemoglobins – (with a fundamental involvement of the distal histidine), as well as by added anion concentrations – suggesting either a process dominated by nucleophilic displacement of superoxide for AtHb2 or an inhibitory effect for AtHb1 and AtHb3. Reducing agents, such as ascorbate and glutathione, are found to either enhance– (presumably via direct electron transfer or via allosteric regulation) or prevent autoxidation. HbFe3+ reduction was possible in the presence of high (presumably not physiologically relevant) concentrations of NADH, glutathione and ascorbate, with differing behaviors for the three globins. The iron coordination sphere is found to affect the autoxidation, redox state interconversion and redox potentials in these three phytoglobins.

Smart Materials Meet Multifunctional Biomedical Devices: Current and Prospective Implications for Nanomedicine.

With the increasing advances in the fabrication and in monitoring approaches of nanotechnology devices, novel materials are being synthesized and tested for the interaction with biological environments. Among them, smart materials in particular provide versatile and dynamically tunable platforms for the investigation and manipulation of several biological activities with very low invasiveness in hardly accessible anatomical districts. In the following, we will briefly recall recent examples of nanotechnology-based materials that can be remotely activated and controlled through different sources of energy, such as electromagnetic fields or ultrasounds, for their relevance to both basic science investigations and translational nanomedicine. Moreover, we will introduce some examples of hybrid materials showing mutually beneficial components for the development of multifunctional devices, able to simultaneously perform duties like imaging, tissue targeting, drug delivery, and redox state control. Finally, we will highlight challenging perspectives for the development of theranostic agents (merging diagnostic and therapeutic functionalities), underlining open questions for these smart nanotechnology-based devices to be made readily available to the patients in need.

A lack of GluN2A-containing NMDA receptors confers a vulnerability to redox dysregulation: Consequences on parvalbumin interneurons, and their perineuronal nets

The GluN2A subunit of NMDA receptors (NMDARs) plays a critical role during postnatal brain development as its expression increases while Glun2B expression decreases. Mutations and polymorphisms in GRIN2A gene, coding for GluN2A, are linked to developmental brain disorders such as mental retardation, epilepsy, schizophrenia. Published data suggest that GluN2A is involved in maturation and phenotypic maintenance of parvalbumin interneurons (PVIs), and these interneurons suffer from a deficient glutamatergic neurotransmission via GluN2A-containing NMDARs in schizophrenia.In the present study, we find that although PVIs and their associated perineuronal nets (PNNs) appear normal in anterior cingulate cortex of late adolescent/young adult GRIN2A KO mice, a lack of GluN2A delays PNN maturation. GRIN2A KO mice display a susceptibility to redox dysregulation as sub-threshold oxidative stress and subtle alterations in antioxidant systems are observed in their prefrontal cortex. Consequently, an oxidative insult applied during early postnatal development increases oxidative stress, decreases the number of parvalbumin-immunoreactive cells, and weakens the PNNs in KO but not WT mice. These effects are long-lasting, but preventable by the antioxidant, N-acetylcysteine. The persisting oxidative stress, deficit in PVIs and PNNs, and reduced local high-frequency neuronal synchrony in anterior cingulate of late adolescent/young adult KO mice, which have been challenged by an early-life oxidative insult, is accompanied with microglia activation.Altogether, these indicate that a lack of GluN2A-containing NMDARs alters the fine control of redox status, leading to a delayed maturation of PNNs, and conferring vulnerability for long-term oxidative stress, microglial activation, and PVI network dysfunction.

RNA Exosome Complex-Mediated Control of Redox Status in Pluripotent Stem Cells.

SummaryThe RNA exosome complex targets AU-rich element (ARE)-containing mRNAs in eukaryotic cells. We identified a transcription factor, ZSCAN10, which binds to the promoters of multiple RNA exosome complex subunits in pluripotent stem cells to maintain subunit gene expression. We discovered that induced pluripotent stem cell clones generated from aged tissue donors (A-iPSC) show poor expression of ZSCAN10, leading to poor RNA exosome complex expression, and a subsequent elevation in ARE-containing RNAs, including glutathione peroxidase 2 (Gpx2). Excess GPX2 leads to excess glutathione-mediated reactive oxygen species scavenging activity that blunts the DNA damage response and apoptosis. Expression of ZSCAN10 in A-iPSC recovers RNA exosome gene expression, the DNA damage response, and apoptosis. These findings reveal the central role of ZSCAN10 and the RNA exosome complex in maintaining pluripotent stem cell redox status to support a normal DNA damage response.

Electrochemical Investigations of the Mechanism of Assembly of the Active-Site H-Cluster of [FeFe]-Hydrogenases.

Protein film electrochemistry (PFE) has been used to study the assembly of the complex 6Fe active site of [FeFe]-hydrogenases (known as the H-cluster) from its precursors-the [4Fe-4S] domain that is already coordinated within the host, and the 2Fe domain that is presented as a synthetic water-soluble complex stabilized by an additional CO. Not only does PFE allow control of redox states via the electrode potential but also the immobilized state of the enzyme facilitates control of extremely low concentrations of the 2Fe complex. Results for two enzymes, CrHydA1 from Chlamydomonas reinhardtii and CpI from Clostridium pasteurianum, are very similar, despite large differences in size and structure. Assembly begins with very tight binding of the 34-valence electron 2Fe complex to the apo-[4Fe-4S] enzyme, well before the rate-determining step. The precursor is trapped under highly reducing conditions (<-0.5 V vs SHE) that prevent fusion of the [4Fe-4S] and 2Fe domains (via cysteine-S) since the immediate product would be too electron-rich. Relaxing this condition allows conversion to the active H-cluster. The intramolecular steps are relevant to the final stage of biological H-cluster maturation.

Understanding butanol tolerance and assimilation in Pseudomonas putida BIRD-1: an integrated omics approach.

Pseudomonas putida BIRD-1 has the potential to be used for the industrial production of butanol due to its solvent tolerance and ability to metabolize low-cost compounds. However, the strain has two major limitations: it assimilates butanol as sole carbon source and butanol concentrations above 1% (v/v) are toxic. With the aim of facilitating BIRD-1 strain design for industrial use, a genome-wide mini-Tn5 transposon mutant library was screened for clones exhibiting increased butanol sensitivity or deficiency in butanol assimilation. Twenty-one mutants were selected that were affected in one or both of the processes. These mutants exhibited insertions in various genes, including those involved in the TCA cycle, fatty acid metabolism, transcription, cofactor synthesis and membrane integrity. An omics-based analysis revealed key genes involved in the butanol response. Transcriptomic and proteomic studies were carried out to compare short and long-term tolerance and assimilation traits. Pseudomonas putida initiates various butanol assimilation pathways via alcohol and aldehyde dehydrogenases that channel the compound to central metabolism through the glyoxylate shunt pathway. Accordingly, isocitrate lyase - a key enzyme of the pathway - was the most abundant protein when butanol was used as the sole carbon source. Upregulation of two genes encoding proteins PPUBIRD1_2240 and PPUBIRD1_2241 (acyl-CoA dehydrogenase and acyl-CoA synthetase respectively) linked butanol assimilation with acyl-CoA metabolism. Butanol tolerance was found to be primarily linked to classic solvent defense mechanisms, such as efflux pumps, membrane modifications and control of redox state. Our results also highlight the intensive energy requirements for butanol production and tolerance; thus, enhancing TCA cycle operation may represent a promising strategy for enhanced butanol production.

Control of Trx1 redox state modulates protection against methyl methanesulfonate-induced DNA damage via stabilization of p21.

Thioredoxin 1 (Trx1) is known to play an important role in protecting against cell death. However, the mechanism for control of Trx1 in cell death resulting from DNA damage has not been fully investigated. In this study, we used the DNA-damaging agent methyl methanesulfonate (MMS) to investigate the protective effects of Trx1 against DNA damage and cell death in HEK293 cells. We found that MMS application caused dose-dependent changes in the Trx1 redox state determined by redox western blotting. At lower concentrations, both reduced and oxidized Trx1 were observed, whereas the reduced band was fully oxidized at the higher concentration. Trx1 overexpression and small interfering RNA knockdown in cells revealed that reduced Trx1 after exposure to lower doses of MMS attenuated DNA damage, assessed by comet assay, and level of the DNA-damage marker histone γ-H2AX, possibly through scavenging intracellular ROS and an increase in p21 protein level via enhancing its stability. However, oxidized Trx1 lost its protective ability to DNA damage in response to higher concentration of MMS. Corresponding to the redox state control of Trx1, cell death induced by different dose of MMS was also found, by inhibiting phosphorylations of p38 and 4E-BP1. These results indicate that reduced Trx1 plays important protective roles against MMS-induced DNA damage and cell death, suggesting that cell protection is regulated by the intracellular redox state. Control of the redox state of Trx1 and its regulating proteins may offer a novel therapeutic strategy for the control of cancer.

Redox state control of a metalloprotein to generate multi-level signals for applications to bioelectronic devices

In this research, we investigate the redox state control of metalloprotein immobilized on a metal surface for the generation of different output signals. Ferredoxin, as a type of metalloprotein, is immobilized on an Au substrate by a chemical linking method using organic materials for the fabrication of a stable protein thin film. To control ionic state of the immobilized ferredoxin, the external electrochemical potentials for oxidation and reduction are applied selectively to the ferredoxin layer. The initial output signal is enhanced or suppressed by the reverse potential, which can inhibit electron transfer by restricting the number of redoxreactive molecules. Consequently, multi-level signals are achieved using a single protein film, and this proposed concept can be used widely to fabricate biosensors for multi-target detection and bioelectronic devices with new functionalities.